Tinnitus is any sound perceived to be coming from the head or ears without an external sound source. Tinnitus is a distressing symptom affecting up to 30% of the population, with 2-4% severely debilitated. Any lesion along the tonotopically organized auditory tract, influencing its normal function, can generate tinnitus. The layout of the auditory tract is genetically determined but its tonotopy arises in response to sensory input during critical periods of early development. Any alteration of the normal sensory input in the fully developed auditory system leads to a reorganization of the entire auditory tract starting peripherally and ending cortically. This reorganization occurs in two phases and it follows the same Darwinian rules that apply for the developmental organization of the auditory system.
After frequency selective monaural cochlear or auditory tract lesions, the tonotopic map in the brainstem nuclei and auditory cortex can reorganize within one to three hours such that cortical neurons deprived of their usual afferent input become supersensitive and then respond to tone frequencies adjacent to the frequency range damaged by the lesion (lesion-edge frequencies). Tinnitus most probably arises when auditory cortical cells are processing auditory input for which they are not predestined. The tonotopic maps for input from each ear can be independently modified, so that a lesion in one ear results in an altered cortical map contralaterally, while the tonotopic map of the intact cochlea remains unaltered. This produces a tonotopic mismatch that can be visualised using magnetic source imaging. Furthermore there is a high positive association between subjective tinnitus strength and the amount of shift of the tinnitus frequency in the auditory cortex. This is similar to the amount of reorganization of the somatosensory cortex and the amount of phantom limb pain.
Since little is known on the pathophysiology of tinnitus, a closer look at the pathophysiology of phantom pain can facilitate a better understanding of tinnitus. The “gate control” theory proposes that a “pain gate” exists in the dorsal horns in the spinal cord. This gate is either open or closed for transmission of painful stimuli to the brain. Whether the gate is open or closed depends on a balance of small (c-fibers) and large fibers (Aα and Aβ). The gate would open, thus giving rise to the subjective feeling of pain, in response to an excess of small fiber activity and close in response to predominantly large fiber activity. These large fibers have a lower threshold for depolarization to an electrical stimulus and can thus be selectively recruited. Therefore electrical treatment stimulating these large fibers selectively can change the balance between small and large fiber afferents, thus closing the pain gate. Based on this principle, spinal cord stimulation is used ever more frequently for patients with phantom pain. As the amount of phantom pain is strongly correlated with the amount of reorganization in the somatosensory cortex, we would expect this reorganization to reverse in patients successfully treated with spinal cord stimulation for phantom pain. This reorganization is exactly what has been observed in patients with neuropathic pain who become pain free after spinal cord stimulation as demonstrated by magnetoencephalography (MEG).
Tinnitus can be treated with electrical stimulation, transcutaneously, at the promontory or with a cochlear implant. Results vary but the more central the stimulation, the more reduction in tinnitus can be observed.
Based on the anatomy (tonotopic organization of dorsal cochlear nucleus and cortex), the pathophysiology (gate control hypothesis and auditory tract reorganization) and the clinical results of electrical stimulation (cochlear implants), it can be theoretically hypothesized that brainstem and auditory cortex stimulation may have an effect on tinnitus relief in patients with or without significant hearing loss. Stimulating selectively, the frequency of hearing loss or the tinnitus level should prevent reorganization at the brainstem and at the auditory tract all the way up to the auditory cortex, thus preventing or treating the tinnitus as long as reorganization has not yet reached the second phase of irreversible cortical, thalamocortical and corticothalamic connection formation. This implies that tinnitus should be treated as soon as possible, preferably within a few years of onset. This does not mean that this procedure will not work for patients who have had tinnitus for longer durations, but it is possible that treatment may be less effective. Indirect arguments for not delaying treatment for tinnitus come from results of microvascular decompressions performed in the treatment of neurovascular compression tinnitus. There is a clear correlation between the duration of tinnitus and the success rate of the surgical decompression.
In one study the effects of electrical brainstem stimulation on tinnitus were analyzed in bilaterally deaf NF-2 patients with brainstem implants placed for auditory stimulation. The tinnitus was improved in eight of ten patients, suggesting prospective studies with brainstem stimulation are waranted.
In phantom pain, motor cortex stimulation is used as a treatment option. Similarly, auditory cortex stimulation may help relieve tinnitus. Its working mechanism seems to rely on cortico-thalamic connections, and not on cortical neurons or somatosensory neurons as demonstrated by PET studies. Thus stimulating the auditory cortex, lateral lemniscus, the inferior olive, medial geniculate body, dorsal cochlear nucleus, the cochlear nucleus and the superior olive either alone or separately could activate cortico-thalamic connections resulting in thalamic reorganization, with relief of tinnitus as a result.
There is currently no cure for tinnitus. There are several modalities that may be of benefit to some patients. These include: vitamin and herbal therapies, masking techniques, pharmacologic strategies (focused primarily on anxiolytics and antidepressants), tinnitus retraining therapy, and complementary and integrative therapies (i.e., acupuncture, hypnotherapy, biofeedback).
U.S. Pat. No. 5,697,975 teaches that electrical stimulation to the brain, specifically the auditory cortex will eliminate tinnitus. This is true only in part: The tinnitus will likely be decreased for a short period of time i.e., 1-4 days. Then the brain reorganizes and the tinnitus returns. Thus, there is a need for such a tinnitus treatment.
Moreover, in treatment of tinnitus by electrical stimulation of the brain there is a need for improving methods of localizing the stimulation areas within the brain.